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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The Tof1p-Csm3p protein complex counteracts the Rrm3p helicase to control replication termination of Saccharomyces cerevisiae
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The Tof1p-Csm3p protein complex counteracts the Rrm3p helicase to control replication termination of Saccharomyces cerevisiae

机译：Tof1p-Csm3p蛋白复合物抵消Rrm3p解旋酶以控制酿酒酵母的复制终止

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摘要

Termination of replication forks at the natural termini of the rDNA of Saccharomyces cerevisiae is controlled in a sequence-specific and polar mode by the interaction of the Fob1p replication terminator protein with the tandem Ter sites located in the nontran-scribed spacers. Here we show, by both 2D gel analyses and chromatin immunoprecipitations (ChIP), that there exists a second level of global control mediated by the intra-S-phase checkpoint protein complex of Tof1p and Csm3p that protect stalled forks at Ter sites against the activity of the Rrm3p helicase ("sweepase"). The sweepase tends to release arrested forks presumably by the transient displacement of the Ter-bound Fob1p. Consistent with this mechanism, very few replication forks were arrested at the natural replication termini in the absence of the two checkpoint proteins. In the absence of the Rrm3p helicase, there was a slight enhancement of fork arrest at the Ter sites. Simultaneous deletions of the TOF1 (or CSM3), and the RRM3 genes restored fork arrest by removing both the fork-releasing and fork-protection activities. Other genes such as MRC1, WSS1, and PSY2 that are also involved in the MRC1 checkpoint pathway were not involved in this global control. This observation suggests that Tof1p-Csm3p function differently from MRC1 and the other above-mentioned genes. This mechanism is not restricted to the natural Ter sites but was also observed at fork arrest caused by the meeting of a replication fork with transcription approaching from the opposite direction.
机译：Fob1p复制终止子蛋白与位于非转录间隔区中的串联Ter位点的相互作用，以序列特异性和极性模式控制了酿酒酵母rDNA天然末端的复制叉终止。在这里，我们通过2D凝胶分析和染色质免疫沉淀（ChIP）显示，存在由Tof1p和Csm3p的S期内关卡蛋白复合物介导的第二级全局控制，该复合物可保护Ter位点的停滞叉子免受活性影响Rrm3p解旋酶（“清扫酶”）的表达。扫掠酶可能是由于Ter结合的Fo​​b1p的瞬时位移而倾向于释放被捕的叉子。与这种机制一致，在没有两个检查点蛋白的情况下，很少有复制叉被停在天然复制末端。在不存在Rrm3p解旋酶的情况下，在Ter部位的叉形逮捕稍有增强。 TOF1（或CSM3）和RRM3基因的同时缺失通过消除叉的释放和叉保护的作用恢复了叉的停滞。也与MRC1检查点途径有关的其他基因，例如MRC1，WSS1和PSY2，不参与此全局控制。该观察结果表明，Tof1p-Csm3p的功能不同于MRC1和其他上述基因。该机制不仅限于天然Ter位点，而且在由复制叉相遇而引起的叉停滞中也观察到，转录从相反方向接近。

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